We can speculate that this can be due to different pathogenic mechanisms underlying myocarditis: prevalent overactivation of the immune system in patients without comorbidities, who showed a higher level of IL-6 and who responded earlier to corticosteroid therapy; prevalent direct viral damage and pathologic changes to the renin-angiotensin-aldosterone system[24] in patients with comorbidities, who were older, had a higher rate of cardiac diseases and needed longer support of inotropic therapy. This evidence concerns the gene IL6 and heart disorder.